Bacterial infection triggers Wnt signaling and upregulates gcFGF8a, which is consistent with previous reports that Wnt/β‐catenin pathway activation increases FGF8 expression.[55] Our findings also revealed that acute skin injuries induce a hypoxic microenvironment in teleosts, marked by increased HIF1α expression.[34] Additionally, during wound healing, the expression levels of HIF1α and gcFGF8a synchronously increased, suggesting a potential association. This evidence concerns the gene FGF8 and bacterial infectious disease.